δ-opioid Receptor Mobilization of Intracellular Calcium in SH-SY5Y Cells: Lack of Evidence for δ-receptor Subtypes

Connor, Mark; Keir, Miranda J; Henderson, Graeme

doi:10.1016/s0028-3908(96)00144-x

Cited by 24 publications

(19 citation statements)

References 19 publications

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“…(Seward et al, 1990;, decrease levels of cyclic AMP (Kazmi & Mishra, 1987;Yu & Sadee, 1988) and promote the generation of IP3 (Smart et al, 1994) in SH-SY5Y cells through PTX-sensitive G-proteins. (Connor et al, 1995). This is consistent with the properties of the 6 receptor cloned from SH-SY5Y cells, which exhibits a mixed 61/62 pharmacological profile (Simonin et al, 1994 (Jin et al, 1993;1994;Prather et al, 1994b) (Exton, 1994 While opioids do not appear to increase IP3 directly they could, in theory, be acting at any of a number of sites in the muscarinic receptor/PLC cascade to (re)sensitize the Ca2+ mobilization process.…”

Section: Drugs and Chemicalssupporting

confidence: 67%

δ‐ and μ‐opioid receptor mobilization of intracellular calcium in SH‐SY5Y human neuroblastoma cells

Connor

Henderson

1996

British J Pharmacology

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Section: Drugs and Chemicalssupporting

confidence: 67%

δ‐ and μ‐opioid receptor mobilization of intracellular calcium in SH‐SY5Y human neuroblastoma cells

Connor

Henderson

1996

British J Pharmacology

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“…Most of the results about opioid-induced elevation of intracellular Ca 2+ come from the studies in neuronal-like cell lines (e.g., NG108-15, SK-N-SH, NMB, SH-SY5Y, Neuro2a, CHO cell lines) (Jin et al, 1992; Fields et al, 1995; Smart and Lambert, 1996; Spencer et al, 1997; Connor et al, 1997; Yoon et al, 1998, 1999; Harrison et al, 1999; Morikawa et al, 1998, 1999). Though these cells may not be identical to native brain cells, the data yielded from them provide initial clues for understanding the roles of opioid system in regulation of [Ca 2+ ]i and the relevant physiological implications (e.g., regulation of transmitter release) in early research.…”

Section: Role Of Opioid Systems In Ionic Homeostasis Under Normal mentioning

confidence: 99%

Ionic storm in hypoxic/ischemic stress: Can opioid receptors subside it?

Chao

Xia

2010

Progress in Neurobiology

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Neurons in the mammalian central nervous system are extremely vulnerable to oxygen deprivation and blood supply insufficiency. Indeed, hypoxic/ischemic stress triggers multiple pathophysiological changes in the brain, forming the basis of hypoxic/ischemic encephalopathy. One of the initial and crucial events induced by hypoxia/ischemia is the disruption of ionic homeostasis characterized by enhanced K + efflux and Na + -, Ca 2+ -and Cl − influx, which causes neuronal injury or even death. Recent data from our laboratory and those of others have shown that activation of opioid receptors, particularly δ-opioid receptors (DOR), is neuroprotective against hypoxic/ischemic insult. This protective mechanism may be one of the key factors that determine neuronal survival under hypoxic/ ischemic condition. An important aspect of the DOR-mediated neuroprotection is its action against hypoxic/ischemic disruption of ionic homeostasis. Specially, DOR signal inhibits Na + influx through the membrane and reduces the increase in intracellular Ca 2+ , thus decreasing the excessive leakage of intracellular K + . Such protection is dependent on a PKC-dependent and PKA-independent signaling pathway. Furthermore, our novel exploration shows that DOR attenuates hypoxic/ischemic disruption of ionic homeostasis through the inhibitory regulation of Na + channels. In this review, we will first update current information regarding the process and features of hypoxic/ischemic disruption of ionic homeostasis and then discuss the opioid-mediated regulation of ionic homeostasis, especially in hypoxic/ischemic condition, and the underlying mechanisms.

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“…Ca 2ϩ release (Smart et al, 1994(Smart et al, , 1997Smart and Lambert, 1996;Connor et al, 1997;Law et al, 2000;Swevers et al, 2005). To examine the possible effects of ␦-i3L expression on the interaction of various GPCRs with other G proteins, we examined its influence on PLC activation in HEK293 cells expressing the ␦-or -ORs following agonist stimulation.…”

Section: Downloaded Frommentioning

confidence: 99%

“…Previous work on neural SHSY-5Y, neuroblastoma NG108-15, and other cell lines has shown that OR activation leads to increases of Ca 2ϩ mobilization from intracellular stores (Smart and Lambert, 1996;Connor et al, 1997;Swevers et al, 2005). To capitalize on these observations toward the development of a quick and reliable assay for signaling inhibitors, which abolishes downstream G protein signaling via the PLC/Ca 2ϩ pathway upon GPCR activation, we measured the ability of ␦-i3L to influence intracellular Ca 2ϩ mobilization in ␦-and -HEK293 cells following activation of the opioid receptors by the agonists DSLET and DAMGO, respectively.…”

Section: Downloaded Frommentioning

confidence: 99%

Expression of the Third Intracellular Loop of the δ-Opioid Receptor Inhibits Signaling by Opioid Receptors and Other G Protein-Coupled Receptors

Morou

Georgoussi²

2005

J Pharmacol Exp Ther

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To explore the feasibility of developing inhibitors of signaling by opioid receptors and other G protein-coupled receptors (GPCRs) that use the same G protein pool, we investigated the capacity of a minigene encoding the third intracellular loop of the ␦-opioid receptor (␦-i3L) to act as competitive antagonist of the receptor-G protein interface interaction. In ␦-i3L-expressing cells, the peptide blocked high-affinity agonist binding to both the ␦-and the -opioid (␦-OR and -OR) and attenuated opioid and ␣ 2 -adrenergic receptor (␣2AR)-dependent [35 S]guanosine-5Ј-O-(3-thio)triphosphate binding. Furthermore, ␦-i3L expression resulted in inhibition of ␦-, -OR-, and ␣2AR-receptormediated cAMP accumulation, whereas the cAMP response produced by activation of the ␤ 2 -adrenergic receptor was unaffected, suggesting that the inhibitory effects of ␦-i3L expression were selective for G i /G o proteins. Moreover, although ␦-i3L expression also attenuated drastically phospholipase C accumulation and Ca 2ϩ release following -and ␦-OR stimulation, it failed to inhibit carbachol-mediated stimulation of inositol phosphate accumulation in M1-muscarinic receptor-expressing human embryonic kidney 293 cells. Finally, we also examined the effects of ␦-i3L expression on the regulation of the extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase pathway. Our results demonstrate that, although ERK activation by -and ␦-ORs is attenuated by the presence of ␦-i3L, ERK activation mediated by ␣2AR remained unaffected. Collectively, our data demonstrate that the ␦-i3L can be used as potent inhibitor of G protein signaling for various GPCRs that use a common pool of G proteins.

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δ-opioid Receptor Mobilization of Intracellular Calcium in SH-SY5Y Cells: Lack of Evidence for δ-receptor Subtypes

Cited by 24 publications

References 19 publications

δ‐ and μ‐opioid receptor mobilization of intracellular calcium in SH‐SY5Y human neuroblastoma cells

δ‐ and μ‐opioid receptor mobilization of intracellular calcium in SH‐SY5Y human neuroblastoma cells

Ionic storm in hypoxic/ischemic stress: Can opioid receptors subside it?

Expression of the Third Intracellular Loop of the δ-Opioid Receptor Inhibits Signaling by Opioid Receptors and Other G Protein-Coupled Receptors

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